Volume 87, Issue 3, Supplement , Pages 79-81, March 2006
Coronary Artery Disease in Masters-Level Athletes
Article Outline
Abstract
Whiteson JH, Bartels MN, Kim H, Alba AS. Coronary artery disease in masters-level athletes.
Screening athletes and advising them regarding exercise are parts of the practice of physical medicine and rehabilitation. Being able to recognize athletes at risk of coronary events is an important part of preparticipation screening. Good guidelines have been developed that let physicians proceed with confidence in screening and in recommending testing for athletes at risk. This review provides the recommended guidelines for physiatrists in practice.
Overall Article Objectives
(a) To recognize risk of coronary disease in athletes, (b) to identify appropriate screening for people at risk, and (c) to interpret test results in people with coronary disease.
Key Words: Coronary artery disease , Myocardial infarction , Rehabilitation , Sports
REGULAR AEROBIC ACTIVITY positively influences risk factors contributing to the development of atherosclerotic coronary artery disease (CAD), including hypertension, dyslipidemia, and diabetes. Risk for myocardial infarction (MI) and other coronary events may be reduced.1 However, vigorous exercise may cause ischemia, MI, and sudden cardiac death, especially in those unaccustomed to exercise. Overall, the benefits of regular exercise outweigh the risks.
A competitive athlete regularly participates at the highest level within a chosen sport. Achieving excellence requires frequent, intense training. Age and level of participation influence performance expectations and probability of medical issues. Among young athletes, the prevalence of cardiovascular diseases (CVDs) capable of causing sudden death is estimated at 0.3%. With advancing age, CVD is more prevalent and the incidence of significant cardiac complications associated with athletic training and performance is increased. Changes in cardiovascular function and response to exercise training and sports participation associated with aging have been documented previously.2
Sudden death in an athlete is a personal tragedy and significantly affects the involved physicians, the athlete’s family and friends, and the general public. In athletes younger than 35 years, death is most likely caused by hypertrophic cardiomyopathy (HCM) or congenital coronary anomalies.3 In masters-level athletes over the age of 40 years, CAD predominates as a cause of morbidity and sudden death, followed by arrhythmia.4 The prevalence of sudden cardiac death in older athletes approaches 1 in 15,000 joggers and 1 in 50,000 marathon runners.5
Preparticipation screening
Screening masters-level athletes before training and sports participation is essential to identify preexisting CAD and to reduce risk of coronary events.6 In athletes diagnosed with CAD, screening helps determine if athletic performance can be resumed. Screening commences with a history and physical examination (appendix 1).7
A 12-lead electrocardiogram and echocardiography can identify previous MI and other CVDs, including HCM and arrhythmias. A symptom-limited exercise stress test is vital in screening masters-level athletes. Ideally, it should approximate the cardiovascular, metabolic, and mechanical demands of the intended training and sport. An ST-segment depression greater than 1mm denotes ischemia. Athletic risk is associated with the degree of ST depression, hypotensive blood pressure response, ventricular arrhythmias, and reduced exercise capacity. Failure to achieve age-predicted heart rate on the exercise stress test correlates with future cardiac events.8 Cardiac imaging with echocardiography or nuclear perfusion increases sensitivity and specificity of the exercise stress test.
The exercise stress test should be performed with the athlete continuing medications that will be taken during training and competition. Of note, some cardiac medications (eg, β-blockers) are banned substances in selected sports.
Screening for CAD in a disabled athlete, such as a wheelchair athlete or paralympian, requires special consideration. Exercise stress testing with an upper-body ergometer or hand bike may not achieve target heart rates (85% of age- and sex-predicted maximum heart rate) sufficient to maximize the sensitivity and specificity needed to assess for CAD. Pharmacologic myocardial stimulation to the required heart rate is essential, and nuclear imaging is recommended for greatest yield. However, a pharmacologic stress test is not a functional test and does not mimic the physiologic stress of sports participation.
Special consideration is also needed when interpreting exercise-induced electrocardiographic changes in women. Accuracy may be limited by a higher prevalence of resting electrocardiographic changes, a lower prevalence of severe CAD, hormonal factors (endogenous or replacement estrogens) and the inability of many women to exercise to maximum aerobic capacity during stress testing.9, 10
The exercise electrocardiogram’s sensitivity and specificity for detecting CAD in asymptomatic people are lower for women (61% and 70%, respectively) than men (72% and 77%, respectively).11 This difference may result in false-positive exercise stress test results that lead to further unnecessary and more invasive testing or to limitation of or exclusion from sports participation. Adjunctive data from the exercise stress test improves diagnostic accuracy in women. Enhanced heart rate recovery by 1 or 2 minutes after cessation of the test and a greater functional capacity shown on the test have substantial prognostic value. Women with an abnormal resting electrocardiograph or those believed to be at risk for CAD should be considered for echocardiographic or nuclear imaging during the exercise stress test.10
A greater than 50% narrowing of the luminal diameter detected during coronary angiography is significant. In the absence of significant luminal narrowing, intravascular ultrasound (IVUS) identifies subendothelial atherosclerotic plaques at risk of rupture. Measures of coronary calcification by computed tomography correlate with atherosclerosis and risk of coronary events.12 Other screening tools include cardiac magnetic resonance imaging, ambulatory Holter electrocardiography, tilt table, and electrophysiologic stimulation.
Sports classifications
Sports are classified according to the predictable cardiovascular responses and bodily impact expected. All sports are classified as dynamic or static—or a combination of both—as shown in table 1.
Table 1. Cardiovascular Responses to Dynamic and Static Exercise
| Response | Dynamic | Static |
|---|---|---|
| Relative force generation | Small | Large |
| Joint movement | Large | Minimal |
| Change in muscle length | Rhythmic | Minimal |
| Predominant metabolic pathway | Aerobic | Anaerobic |
| Increases in O2 consumption, cardiac output, SV | Marked | Small |
| Systolic blood pressure | Increased | Increased |
| Diastolic blood pressure | Decreased | Increased |
| Left ventricular load | Volume | Pressure |
| Changes after training | ||
| Markedly increased | No to minimal increase | |
| Markedly increased | No to minimal increase | |
| Increased oxidative enzymes | Increased glycolytic enzymes | |
| No change | Increased | |
| Eccentric hypertrophy | Concentric hypertrophy |
The intensity of dynamic and static exercises ranges from low to high. Myocardial oxygen (MVO2) requirement, which is predominantly influenced by heart rate and systolic blood pressure responses, depends on both the intensity and the type of exercise. When MVO2 is exceeded, ischemia develops. Figure 1 presents a matrix in which sports are classified according to peak static and dynamic intensity achieved during competition.13 Although developed for younger athletes, extrapolation of this classification for the masters-level athlete is acceptable. Other factors that influence cardiovascular responses to exercise include electrolyte abnormalities, emotional stress, altitude, humidity, temperature, and training regimens.

Fig 1.
Sports classification matrix, from static to dynamic levels. The increasing dynamic component is defined in terms of the estimated percentage of maximal oxygen consumption (V̇o2max) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percentage of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in green and the highest in red. Blue, yellow, and orange depict low moderate, moderate, and high moderate total cardiovascular demands. NOTE: Higher intensities (V̇o2max/MVC) may be reached during training. *Danger of bodily collision. †Increased risk if syncope occurs. Source: Mitchell et al.13 Reprinted with permission.
Athletes with CAD are placed in 1 of 2 risk categories (table 2). They are considered at substantial risk if any of the risk factors noted are present. For athletes considered at mildly increased risk, low-intensity dynamic (class 1A) and low- to moderate-intensity static (classes 1A and 2A) sports are recommended (see fig 1).14 Masters-level athletes with an overall clinical profile suggesting a very low exercise risk may be allowed to exercise at higher intensity levels. A cautious approach must be taken, with new symptoms prompting a clinical reevaluation and review of the risk categorization. Athletes must be counseled regarding possible symptoms and signs and must be educated about the risk of cardiac events. Athletes stratified as having substantially increased risk are restricted to low-intensity dynamic and static sports (class 1A).
Table 2. Risk Categorization of Athletes with CAD
| Risk Area | Mild Risk | Substantial Risk |
|---|---|---|
| Left ventricular systolic function | Normal. EF >50% | Reduced. EF <50% |
| Exercise tolerance for age⁎ | Normal | Reduced |
| Exercise-induced ischemia | Absent | Present |
| Significant coronary stenosis | Absent | Present |
| Myocardial revascularization | Successful | Incomplete |
⁎ One MET unit implies the consumption of 3.5mL of o2·kg−1·min−1. |
After a recent cardiac event, inpatient and/or outpatient cardiac rehabilitation is recommended. Progression to athletic performance after outpatient cardiac rehabilitation is guided by a postrehabilitation exercise stress test and response to increasing training intensities under monitored settings.
Myocardial ischemia can be caused by coronary vasospasm without atherosclerosis. Low-intensity sports (class 1A) are recommended. Myocardial bridging, in which a coronary vessel tunnels within the myocardium, can also lead to exercise-induced ischemia. However, without evidence of inducible ischemia, all competitive sports are allowed according to documented exercise capacity. With ischemia or history of infarction, only class 1A sports are permissible. After surgical correction of the myocardial bridge, if the exercise stress test results are negative, all sports are allowed. After cardiac transplantation, accelerated coronary atherosclerosis is noted in the donor heart. Cardiac evaluation is complex because of altered physiologic parameters at rest and in response to exercise. The IVUS improves the sensitivity of screening for atherosclerosis. Athletes with no abnormalities detected can participate in all sports. With atherosclerosis, evaluation and stratification is as for those with CAD.
Masters-level athletes should be rescreened annually with noninvasive testing that includes history, physical examination, electrocardiogram, echocardiogram, and exercise stress test. Risk stratification and athletic participation are revised accordingly. New symptoms, signs, or unexpected decline in performance warrant immediate cessation of sports and thorough reevaluation. Education of the athlete regarding risks of sports participation must be emphasized. Legal issues regarding physician recommendations of athletic participation have recently been documented.15
Appendix 1.
American heart association consensus panel recommendations for preparticipation screening7
| Family history |
| Personal history |
| Physical examination |
References
- Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease (a statement from the Council on Clinical Cardiology and the Council on Nutrition, Physical Activity, and Metabolism) . Circulation . 2003;107:3109–3116
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- . Risk for sudden cardiac death associated with marathon running . J Am Coll Cardiol . 1996;28:428–431
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- Cardiovascular preparticipation screening of competitive athletes (A statement for health professionals from the Sudden Death Committee (Clinical Cardiology) and Congenital Cardiac Defects Committee (Cardiovascular Disease in the Young), American Heart Association) . Circulation . 1996;94:850–856
- . Value of maximal exercise tests in risk assessment of primary coronary heart disease events in healthy men . Five years’ experience of the Seattle Heart Watch Study Am J Cardiol . 1980;46:371–378
- ACC/AHA 2002 guideline update for exercise testing. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines) . 2005; http://www.acc.org/clinical/guidelines/exercise/dirIndex.htm. Accessed October 24, 2005
- Role of noninvasive testing in the clinical evaluation of women with suspected coronary artery disease (Consensus statement from the Cardiac Imaging Committee, Council on Clinical Cardiology, and the Cardiovascular Imaging and Intervention Committee, Council on Cardiovascular Radiology and Intervention, American Heart Association) . Circulation . 2005;111:682–696
- . Meta-analysis of exercise testing to detect coronary artery disease in women . Am J Cardiol . 1999;83:660–666
- . Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals . [published erratum in: JAMA 2004;291:563] JAMA . 2004;291:210–215
- . Task Force 8 (classification of sports) . 36th Bethesda Conference J Am Coll Cardiol . 2005;45:1364–1367
- . Task Force 6 (coronary artery disease) . 36th Bethesda Conference J Am Coll Cardiol . 2005;45:1348–1353
- . Task Force 12 (legal aspects of the 36th Bethesda Conference recommendations) . 36th Bethesda Conference J Am Coll Cardiol . 2005;45:1373–1375
Supported in part by the Vidda Foundation.
No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated.
PII: S0003-9993(05)01478-4
doi:10.1016/j.apmr.2005.12.010
© 2006 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.
Volume 87, Issue 3, Supplement , Pages 79-81, March 2006
